Zhang Xingqi, Sliwowska Joanna H, Weinberg Joanne
Department of Cellular and Physiological Sciences, Faculty of Medicine, The University of British Columbia, 2177 Wesbrook Mall, Vancouver, British Columbia V6T 1Z3, Canada.
Exp Biol Med (Maywood). 2005 Jun;230(6):376-88. doi: 10.1177/15353702-0323006-05.
Alcohol abuse is known to result in clinical abnormalities of endocrine function and neuroendocrine regulation. However, most studies have been conducted on males. Only recently have studies begun to investigate the influence of alcohol on endocrine function in females and, more specifically, endocrine function during pregnancy. Alcohol-induced endocrine imbalances may contribute to the etiology of fetal alcohol syndrome. Alcohol crosses the placenta and can directly affect developing fetal cells and tissues. Alcohol-induced changes in maternal endocrine function can disrupt maternal-fetal hormonal interactions and affect the female's ability to maintain a successful pregnancy, thus indirectly affecting the fetus. In this review, we focus on the adverse effects of prenatal alcohol exposure on neuroendocrine and immune function, with particular emphasis on the hypothalamic-pituitary-adrenal (HPA) axis and the concept of fetal programming. The HPA axis is highly susceptible to programming during fetal development. Early environmental experiences, including exposure to alcohol, can reprogram the HPA axis such that HPA tone is increased throughout life. We present data that demonstrate that maternal alcohol consumption increases HPA activity in both the maternal female and the offspring. Increased exposure to endogenous glucocorticoids throughout the lifespan can alter behavioral and physiologic responsiveness and increase vulnerability to illnesses or disorders later in life. Alterations in immune function may be one of the long-term consequences of fetal HPA programming. We discuss studies that demonstrate the adverse effects of alcohol on immune competence and the increased vulnerability of ethanol-exposed offspring to the immunosuppressive effects of stress. Fetal programming of HPA activity may underlie some of the long-term behavioral, cognitive, and immune deficits that are observed following prenatal alcohol exposure.
众所周知，酒精滥用会导致内分泌功能和神经内分泌调节出现临床异常。然而，大多数研究是针对男性进行的。直到最近，研究才开始调查酒精对女性内分泌功能的影响，更具体地说，是对孕期内分泌功能的影响。酒精引起的内分泌失衡可能是胎儿酒精综合征病因的一部分。酒精可穿过胎盘，直接影响发育中的胎儿细胞和组织。酒精引起的母体内分泌功能变化会扰乱母胎激素相互作用，影响女性维持成功妊娠的能力，从而间接影响胎儿。在这篇综述中，我们重点关注产前酒精暴露对神经内分泌和免疫功能的不良影响，特别强调下丘脑 - 垂体 - 肾上腺（HPA）轴以及胎儿编程的概念。HPA轴在胎儿发育过程中极易受到编程影响。早期环境经历，包括接触酒精，可对HPA轴进行重新编程，使HPA张力在一生中都增加。我们提供的数据表明，母体饮酒会增加母体和后代的HPA活性。一生中内源性糖皮质激素暴露增加会改变行为和生理反应性，并增加日后患疾病或失调的易感性。免疫功能改变可能是胎儿HPA编程的长期后果之一。我们讨论了一些研究，这些研究证明了酒精对免疫能力的不良影响以及乙醇暴露后代对应激免疫抑制作用的易感性增加。产前酒精暴露后观察到的一些长期行为、认知和免疫缺陷可能源于胎儿HPA活性的编程。
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